The recurrence of spinal cord compression in the fluorotic spine 20 years after laminectomy is a very unusual event and hence the patient should be kept under observation for a long duration. This case report contributes to the literature associated with the management of fluorotic spine.
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To assess effectiveness and safety of tizanidine hydrochloride tablets for the prophylaxis of chronic daily headache.
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Noradrenergic drugs, acting on alpha adrenoceptors, have been found to play an important role in the initiation and modulation of locomotor pattern in adult cats after spinal cord transection. There are at least two subtypes of alpha adrenoceptors, alpha1 and alpha2 adrenoceptors. The aim of this study was to investigate the effects of selective alpha1 and alpha2 agonists in the initiation and modulation of locomotion in adult chronic cats in the early and late stages after complete transection at T13. Five cats, chronically implanted with an intrathecal cannula and electromyographic (EMG) electrodes were used in this study. Noradrenergic drugs including alpha2 agonists (clonidine, tizanidine, and oxymetazoline) and an antagonist, yohimbine, one alpha1 agonist (methoxamine), and a blocker, prazosin, as well as norepinephrine were injected intrathecally. EMG activity synchronized to video images of the hindlimbs were recorded before and after each drug injection. The results show differential effects of alpha1 and alpha2 agonists in the initiation of locomotion in early spinal cats (i.e., in the first week or so when there is no spontaneous locomotion) and in the modulation of locomotion and cutaneous reflexes in the late-spinal cats (i.e., when cats have recovered spontaneous locomotion). In early spinal cats, all three alpha2 agonists were found to initiate locomotion, although their action had a different time course. The alpha1 agonist methoxamine induced bouts of nice locomotor activity in three spinal cats some hours after injection but only induced sustained locomotion in one cat in which the effects were blocked by the alpha1 antagonist prazosin. In late spinal cats, although alpha2 agonists markedly increased the cycle duration and flexor muscle burst duration and decreased the weight support or extensor activity (effects blocked by an alpha2 antagonist, yohimbine), alpha1 agonist increased the weight support and primarily the extensor activity of the hindlimbs without markedly changing the timing of the step cycle. Although alpha2 agonists, especially clonidine, markedly reduced the cutaneous excitability and augmented the foot drag, the alpha1 agonist was found to increase the cutaneous reflex excitability. This is in line with previously reported differential effects of activation of the two receptors on motoneuron excitability and reflex transmission. Noradrenaline, the neurotransmitter itself, increased the cycle duration and at the same time retained the cutaneous excitability, thus exerting both alpha1 and alpha2 effects. This work therefore suggests that different subclasses of noradrenergic drugs could be used to more specifically target aspects of locomotor deficits in patients after spinal injury or diseases.
Spasticity is a frequently observed motor impairment that develops after stroke; it can cause pain and disability in those affected. The objective of the present study was to evaluate the safety and efficacy of tizanidine, a centrally acting alpha(2)-adrenergic agonist, in the treatment of stroke-related spasticity.
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We evaluated the efficacy of complex treatment in 152 patients with chronic tension-type headache (СЕЕР) and 96 patients with facial MFPS. The treatment included standard methods (reflex therapy of СЕЕР and local injections of a combination of local anesthetics with small doses of steroids in trigger points in patients with facial MFPS. To assess the efficacy of tizanidine, patients were randomized into two comparable groups. The duration of the study was 12 weeks.
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Forty patients scheduled to undergo epidural anesthesia in elective surgery were randomly allocated into two groups. The control group received placebo 60 minutes before arrival in the operating room, and the tizanidine group received 3 mg of oral tizanidine as premedication 60 minutes before arrival in the operating room. Every patient was measured heart rate and blood pressure before receiving placebo or premedication and after arrival in the operating room. After an epidural catheter was indwelled, the patients were questioned about the infiltrating pain of local anesthetic, and the degree was assessed by means of visual analog scale score (VAS score, 0 to approximately 100 mm).
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Ventral spinocerebellar tract neurons located in laminae V-VII of cat lumbar spinal cord were tested for the effects of ionophoretically applied monoamines and receptor selective agonists. Extracellularly recorded responses, monosynaptically evoked by group I afferents in a muscle nerve, were compared before, during, and after ionophoresis. They were analyzed with respect to changes in the number of evoked spikes and in the latency. Both serotonin (5-HT) and noradrenaline (NA) were found to facilitate responses of all neurons tested. Ionophoresis of three serotonin subtype receptor agonists (5-carboxamidotryptamine maleate, 5 methoxytryptamine HCl, and alpha-methyl 5-hydroxytryptamine) and of two NA receptor agonists (phenylephrine and isoproterenol) likewise had a facilitatory effect. However, three other 5-HT receptor agonists (8-hydroxy-dipropylaminotetraline hydrobromide), 2-methyl 5-hydroxytryptamine, and 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl and two NA receptor agonists (tizanidine and clonidine) had the opposite effect because they depressed responses of the tested neurons. These results show that information forwarded by means of the ventral spinocerebellar tract may be modulated by monoamines and that several receptor subtypes, located pre- or postsynaptically, may be involved. The results also demonstrate that transmission by means of group I muscle afferents may not only be facilitated by monoamines but also depressed by selective receptor subtype activation.
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During the past year observations have been published that might lead to further improvement in the design of future clinical trials. At the same time, results of clinical trials have become available that suggest that a number of treatments could be of benefit in the care of patients in the various phases of multiple sclerosis. Future multiple sclerosis clinical trials should involve a blinded investigator restricted to assessing the clinical outcome variables, and because current evidence suggests that magnetic resonance imaging gives an objective and sensitive reflection of the biological evolution of the disease, such scanning should also be included. The use of a composite outcome variable in a trial of chronic progressive multiple sclerosis should also be considered in order to increase the percentage of patients reaching the clinical endpoint. In 1994 recommendations were published for the selection of relapsing-remitting patients for treatment with interferon beta-1b; furthermore, large and well performed clinical trials demonstrated that interferon beta-1a and copolymer-1 are also partially effective, though not curative, for these patients. Two smaller studies suggested that low-dose methotrexate and cladribine might have a beneficial effect on the course of the disease in patients with secondary chronic progressive multiple sclerosis, the former drug probably being less toxic. Unfortunately, therapeutic perspectives for patients with primary progressive multiple sclerosis are less promising at present. Several studies suggest that 4-aminopyridine and tizanidine have therapeutic potential for symptomatic treatment; the former by improving neurological deficits, the latter by relieving troublesome spasticity.(ABSTRACT TRUNCATED AT 250 WORDS)
The patient with mitochondrial encephalomyopathy had left upper- and lower-extremity intention myoclonus; the patient with stroke had left upper intention myoclonus; and the patient with MS had right upper- and left lower-intention myoclonus. In the patient with mitochondrial encephalomyopathy, the FIM score increased from 90 to 103 points over 2 days of tizanidine. The stroke patient's FIM score improved only from 74 to 79 after 4 weeks of tizanidine. The patient with MS improved from 83 to 101 after 6 days of tizanidine. All 3 patients had almost full resolution of the intention myoclonus. All continued on tizanidine except the patient with stroke, who had minimal gains and a low systolic blood pressure. None of the patients experienced significant sedation or hypotension.
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Ciprofloxacin increased the area under the plasma concentration-time curve from time 0 to infinity [AUC(0-infinity)] of tizanidine by 10-fold (range, 6-fold to 24-fold; P < .001) and its peak concentration by 7-fold (range, 4-fold to 21-fold; P < .001), whereas its elimination half-life was only prolonged from 1.5 to 1.8 hours (P = .007). The pharmacodynamic effects of tizanidine were much stronger during the ciprofloxacin phase than during the placebo phase with regard to changes in systolic blood pressure (-35 mm Hg versus -15 mm Hg, P = .001), diastolic blood pressure (-24 mm Hg versus -11 mm Hg, P < .001), Digit Symbol Substitution Test (P = .02), subjective drug effect (P = .002), and subjective drowsiness (P = .009). The AUC(0-infinity) of tizanidine and its change correlated (P < .01) with the caffeine/paraxanthine ratio and its change.
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The analysis of treatment effectiveness was carried out in 138 patients with tension headache. Patients of group 1 received fluoxetine in dose 20-40 mg/day during not less than 3 months and tizanidini in dose 4-8 mg/day during not less than 2 weeks. Patients of group 2 were assigned to therapeutic blockades of the occipital nerve and trigger points of cervico-cranial area using local anesthetics (2.5 ml of 0.5% marcain solution and 0.5-1 ml dexazone, for 1-5 blockades course) and needle reflexotherapy. The further treatment was based on the decision of the necessity of using analogous drugs in dose regime. Effectiveness was assessed on the basis of clinical neuroorthopedical examination, scores on the Visual Analogous Scale and questionnaires of McGill and A.M. Vein. The inclusion of therapeutic blockades of the cervical zone and reflexotherapy increased the effectiveness of the treatment and minimized the use of drugs. In group 2, the amount of analgesics was decreased by more than 60%, central myorelaxants were prescribed in 34.8% of cases and antidepressants - in 19.1%. The decrease of daily and course doses of the drugs allowed to completely avoid the side-effects.
Both LTT and TizLTT resulted in significant improvements in walking speed and dorsiflexion maximum strength, with no significant differences between them, using group-averaging analysis. However, using the MID analysis, a higher proportion of subjects in the TizLTT group achieved the MID for walking speed (40%) compared with LTT alone (13%). Those that achieved the MID for walking speed were significantly higher functioning at baseline than those that did not in the TizLTT group, and the change in walking speed was associated with the change in dorsiflexion peak velocity (R(2) = 0.40; P < 0.05).
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To identify the drug treatments currently available for the management of spasticity and pain in multiple sclerosis (MS), and to evaluate their clinical and cost-effectiveness.
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A comprehensive search and review of the published literature was undertaken.
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Tizanidine, an alpha-2 adrenergic agonist, is a centrally active muscle relaxant and a spasmolytic drug. The aim of our study was to investigate the activity of tizanidine on maximal electroshock seizures (MES) in mice. In the first part of the study, convulsive current 50 (CC 50) value to produce seizures was found. Then, tizanidine was given intraperitoneally (IP) at the doses of 0.5, 1, and 2 mg/kg, and orally (PO) at the doses of 5, 10, 20, 40 mg/kg. We found that tizanidine at the doses of 1 and 2 mg/kg IP and 40 mg/kg PO caused a significant protection against MES. In the second part of the study, after pretreatment with yohimbine, an alpha-2 adrenergic receptor blocker, at the dose of 2 mg/kg, anticonvulsant effect of tizanidine is diminished. We concluded that the mode of action of the anticonvulsant effect of tizanidine may be mediated by the central alpha-2 adrenergic receptors.
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A 33-year-old man with AIDS-related PML developed very severe spastic paraparesis (Ashworth rigidity score, 4) and painful muscle spasms. The patient was unable to sit in his wheelchair and remained bed bound. Combined oral baclofen and tizanidine at therapeutical doses were used without any effect on the spasticity. The patient refused the placement of an intrathecal catheter for long-term baclofen infusion. A single intrathecal ethanol (6 ml) injection in the L2-L3 intervertebral space with the patient placed in a lateral Trendelenburg (40 C) position was performed.
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One hundred forty-two patients with spastic MS who were not taking any interfering medication, such as an antispasticity drug or other alpha-noradrenergic agonist, entered the trial.
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Tizanidine (Sirdalud) was compared to baclofen (Lioresal) in a randomized, double-blind, cross-over trial. Each medication was introduced over a three week titration period and then maintained at the highest tolerated dose for five weeks. The two treatment phases were separated by a one week drug withdrawal and a two week washout period. Sixty-six patients entered the trial and forty-eight completed both treatment phases. At the end of the trial, neurologists and physiotherapists thought that baclofen was superior on the basis of perceived efficacy and tolerance (p less than or equal to 0.05). Although the efficacy of tizanidine or baclofen was judged as good to excellent by 24 and 39% of patients respectively, this difference was not statistically significant. Muscle weakness was the most common adverse effect. This was significantly more troublesome in patients treated with baclofen. Somnolence and xerostomia were more common in patients treated with tizanidine. Both baclofen and tizanidine appear to be useful adjuncts in the treatment of spasticity in patients with multiple sclerosis. Preference of either drug is tempered principally by side-effects.
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Randomised controlled trials (RCTs) of anti-spasticity agents were identified using MEDLINE, EMBASE, bibliographies of relevant articles, personal communication, manual searches of relevant journals and information from drug companies.
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The effects of tizanidine were studied in patients with spastic paresis. The study consisted of 4 parts: I, double-blind cross-over trial at maximal dosage 10 mg/day in 13 patients; II, open trial at maximal dosage 32 mg/day in 10 patients; III, long-term medication at dosage 32 mg/day for 6-15 months in 4 patients; IV, single dose (12 mg) administration in 3 patients. The effects were evaluated from clinical examinations, subjective assessments, EMG, gait analysis and quantitative determinations of passive resistance and voluntary strength in isokinetic extensions and flexions of the knee and plantar and dorsal flexions of the ankle at different speeds of motion. At 3-10 mg/day, no effects were observed except for increased prime mover EMG activity in voluntary knee flexions. At 12-32 mg/day, passive resistance decreased significantly in 3 of the movements tested. The maximal voluntary strength increased significantly in 3 movements, frequently associated with enlarged activation of prime mover muscles, less frequently with reduced antagonist co-activation. Functional disability was subjectively reduced and verified by improved gait capacity in 4 patients. Sustained effects on motor performance during long-term medication were verified by withdrawal in 3 patients. Single dose administration resulted in reduced passive resistance and increased voluntary strength, associated with an increased activation of the prime mover muscles. The results indicate that tizanidine exerts its effects in part by reducing spastic restraint, in part by enhancing the capacity to activate paretic muscles.
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Alpha-2-adrenergic agonists, such as clonidine, produce antinociception in animal pain models after intrathecal administration. However, clinical usage is limited by cardiovascular side effects. To investigate alternative alpha(2)-adrenergic agonists as analgesics, we implanted six dogs with an intrathecal catheter and infusion pump. After baseline saline infusion, animals received clonidine or tizanidine (crossover study) each week at escalating doses of 125-750 microg/h. Analgesia, blood pressure, heart rate, respiratory rate, sedation, and coordination were evaluated. A 28-day safety study was performed with another nine dogs receiving intrathecal tizanidine (3 or 6 mg/d) or saline. Equal doses of clonidine and tizanidine produce the same antinociception in thermal withdrawal tests. Blood pressure was reduced with 125-500 microg/h of clonidine, but not with tizanidine at any dose. Clonidine 250 microg/h reduced heart rate by 45.8%, and five of six animals had bradyarrhythmias (marked bradycardia), whereas tizanidine decreased heart rate by 15.1% without arrhythmias, even at the largest dose. Respiratory rate decreased with 250 microg/h of clonidine and larger doses. Sedation or incoordination occurred only at the largest dose for either drug. The safety study indicated that 3 mg/d of tizanidine in dogs produced no side effects or histopathologic changes. Tizanidine may be a useful alternative in patients experiencing cardiovascular side effects with intrathecal infusion of clonidine.
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Male SD rats weighing 250-300 g were randomly divided into 5 groups (n = 6), namely the control group, ouabain group, tizanidine group, combined ouabain and tizanidine injection group, and the antagonist group. Intrathecal catheter was implanted 7 days before spinal nerve ligation to establish the neuropathic pain model. Mechanical withdrawal threshold (MWT) before and after intrathecal administration of the agents was recorded in the rats. Isobolographic analysis was performed to evaluate the interactions between the agents.
Given the absence of papers on the use of tizanidine hydrochloride in the treatment of myofascial pain of the masticatory muscles, the present investigation could provide some preliminary data about its possible efficacy. Randomized and controlled clinical trials are needed to confirm these results.
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We report a case of profound symptomatic bradycardia after a single dose of tizanidine.